According to the World Health Organization: “Gender refers to the characteristics of women, men, girls and boys that are socially constructed. This includes norms, behaviors and roles associated with being a woman, man, girl or boy, as well as relationships with each other. As a social construct, gender varies from society to society and can change over time.”
A social construct, by its very nature, cannot be innate to human beings and social stereotypes of male and female behaviors are widely variant between cultures and societies. It is blatantly illogical that cultural stereotypes of male and female behaviors could be innate. As discussed in a previous PITT article, the identity disconnect is caused by neuroplastic resting state functional connectivity networks in the brain, which have multiple influences based on a person’s experiences after birth. And yet, many people truly believe that there is such a thing as a soul-like gender identity, and that gender identity is innate – this is gender ideology.
So where did this theory (or myth) of the innate gender identity come from and how is it being continued to be propagated leading to continued confusion in young impressionable minds? As the dad of a gender confused teen son who truly believes in the ideology, I decided to take a look at the concept. Turns out, as usual in the world of trans “medicine”, this concept is based on flawed science, even more flawed analysis of said science, and then ridiculous leaps of logic on top of all that.
In a 1995 paper in Nature, Swaab et al examined slices of brain tissue from 42 people, including six who were born male but attempted to change their sex later in life with the help of plastic surgery and “feminizing” hormones, such as estrogen. The INAH3 or third interstitial nucleus of the anterior hypothalamus, is the sexually dimorphic nucleus of humans, ie, there are differences between men and women in this space. The theory was that if a male really had the brain of female, their INAH3 would look more female than male. Only one major difference came to light between the brains of normal males and those who had changed sex. A tiny cluster of cells known as the “bed nucleus of the stria terminalis”, or BST, was half the size in transsexual men as it was in normal men. Because of this finding, it was promoted as a major factor in cross gender ideation. However, as it has been shown in Chung et al, this nucleus does not show sexually dimorphic differences until well into adulthood and cannot explain the most common modern day onset years of gender confusion before or at puberty. So it cannot be the “innate” cause of gender identity confusion.
In 2008, the same researchers doubled down in a new paper trying to assess if brain differences in trans identified individuals were innate or caused by trans medicine interventions. They found that “The castrated men had an INAH3 volume and neuron number that was intermediate between males (volume and number of neurons P > 0.117) and females (volume P > 0.245 and number of neurons P > 0.341). There was no difference in INAH3 between pre-and post-menopausal women, either in the volume (P > 0.84) or in the number of neurons (P < 0.439), indicating that the feminization of the INAH3 of male-to-female transsexuals was not due to estrogen treatment. We propose that the sex reversal of the INAH3 in transsexual people is at least partly a marker of an early atypical sexual differentiation of the brain and that the changes in INAH3 and the BSTc may belong to a complex network that may structurally and functionally be related to gender identity”. Plainly stated, the castrated males, as they called them, had INAH3 sizes that were somewhere in between those of typical male and female brains.
Now, Dr. Swaab is considered a world renowned neuroscientist and this research got picked up and referred widely to show that people desiring sex change had innately different brain morphology. This is the research underpinning the myth that continues to be promoted to this day through gender ideology.
The problem with all this is that more recent studies clearly demonstrate that exogenous estrogen in males shrinks the brain, as discussed in detail in Transgender Medical Interventions: Impacts on the Brain, Part II. As Gomez et al have shown, this is likely due to water leaching from astrocytes, the glial cells that are abundantly found in the brain—this smaller brain is therefore clearly not innate, but rather caused by the trans medicine treatment. The observations of volume and size between male and female brains can clearly be attributed to this water-leaching caused shrinkage. Given these studies Dr. Swaab’s research is deeply flawed in its methods and conclusions and it did not prove any innateness of “gender identity”.
There were also studies that seem to point to sexual orientation as being visible or maybe innate in the male brain, further muddling the conflation of these issues. In 1991, LeVay published “A difference in hypothalamic structure between heterosexual and homosexual men” in Science. On average, LeVay found that the INAH3 in the brains of heterosexual men were more than twice as large as that found in the homosexuals. In fact, the INAH3 size of the homosexual group was the same size as the women. LeVay wrote that “This finding indicates that INAH is dimorphic with sexual orientation, at least in men, and suggests that sexual orientation has a biological substrate.”
LeVay’s finding attracted a lot of media attention. The study results were featured on PBS, Newsweek, Nightline, Donahue, and The Oprah Winfrey Show. Due to several confounding factors including HIV, small sample size, small size of the INAH-3 brain structure (0.1-0.15mm2), methodological concerns, the brain slicing research received substantial criticism and was discredited as indicating anything substantial. LeVay himself cautioned against misinterpreting his findings.
Finally, however, Byne et al debunked the INAH-3 related gender and sexual orientation myths once and for all. As they observed, “The interstitial nuclei of the human anterior hypothalamus (INAH1–4) have been considered candidates for homology with the sexually dimorphic nucleus of the preoptic area of the rat. Volumetric sexual dimorphism has been described for three of these nuclei (INAH1–3), and INAH3 has been reported to be smaller in homosexual than heterosexual men.
The current study measured the INAH in autopsy material from 34 presumed heterosexual men (24 HIV− and 10 HIV+), 34 presumed heterosexual women (25 HIV− and 9 HIV+), and 14 HIV+ homosexual men. HIV status significantly influenced the volume of INAH1 (8% larger in HIV+ heterosexual men and women relative to HIV− individuals), but no other INAH.
INAH3 contained significantly more neurons and occupied a greater volume in presumed heterosexual males than females. No sex difference in volume was detected for any other INAH. No sexual variation in neuronal size or density was observed in any INAH. Although there was a trend for INAH3 to occupy a smaller volume in homosexual men than in heterosexual men, there was no difference in the number of neurons within the nucleus based on sexual orientation”.
We can’t exclude a conversation about genetics in a review of whether or not “gender identity” is an innate characteristic. Sexual orientation, as many may remember, went down this same path, in terms of research. In an effort to determine if there were genetic origins to sexual orientation, Bailey et al. studied a large population of Monozygotic twins to understand heritability of sexual orientation and cross gender identity in childhood and its persistence in adulthood.
On sexual orientation, the study concluded that “our MZ concordances were 20% (Men) and 24% (Women), respectively. In contrast to most prior twin studies of sexual orientation, however, ours did not provide statistically significant support for the importance of genetic factors for that trait. Our male MZ concordance figure suggests, however, that any major gene for strictly defined homosexuality has either low penetrance or low frequency”.
After several low quality, small sample size, sensationalized studies on this subject, researches at the Nobel Prize awarding Karolinska Institute took another stab at it. However, the study, conducted on nearly half a million subjects, could not identify genetic origins (innateness) of sexuality. In an interview, Melinda Mills, an Oxford University sociologist, said the study is further evidence that previous reports of a “gay gene” on the X chromosome are wrong.
At the same time that they looked at potential genetic causes for sexual orientation, Bailey et al, in their study on monozygotic twins, also looked at cross gender identity and its persistence into adulthood. Of the attributes they studied, they found some limited support for the hypothesis that childhood gender nonconformity is the inherited component of adult sexual orientation development, as indicated earlier by Bem, and expounded later here. They further concluded that only childhood gender nonconformity was significantly heritable for both men and women. However, they also found that this childhood gender nonconformity did not persist into adulthood.
This is consistent with results of cross “gender” identity longitudinal studies in males recently published by Zucker et al, which found that, by age 22, over 80% of males with childhood gender non-conformance had desisted, and that the majority of those studies turned out to be same sex attracted at adulthood. As suggested by these studies, it is clear that cross-gender identity is indeed neuroplastic and changeable, rather than innate and persistent. As such, social and medical interventions in children and adolescents to align one’s changeable cross-gender (stereotypical and undefinable) identity ( “gender”) to an adult sexual orientation is risky and unnecessary, as most desist and many grow up to be gay if left alone by medical providers, and not affirmed in this changeable identity.
Any proof that cross gender identity is biologically innate is completely lacking, and in fact, studies have shown the exact opposite—that it is mutable, and generally resolves by adulthood when interventions are avoided. In a recent interview by NPR of the Los Alamos National Labs scientist Karissa Sanbonmatsu, who has marshaled the world’s largest super computing resources to understand the genetic and epigenetic factors to explain sexuality and cross-gender identity, she clearly indicated that, when it comes to the innate-ness of gender identity “there’s no smoking guns yet at all”. Such an admission will not make the gender ideologues happy.
Now, if we looked into heritability studies of some of the key personality disorders that are found in gender confused children, it maybe possible to explain that childhood gender confusion shares similar higher heritability characteristics as ASD (90%), OCD ( 45-65%), Bipolar Disorder ( 58-87%), and attachment related anxiety (45%)—factors that have been studied and found to contribute to gender identity deficit and confusion in children. This is indeed where any assessment and treatment of childhood GNC should start.
The medical and scientific complexity of this entire discussion makes it incredibly difficult to counter the unethical and ideologically motivated providers and activists who choose to synthesize the abstracts in extremely biased ways, as they always do. And there’s an undeniable appeal to confused teens to think that their distress has a biological, rather than a psychological or society cause. But the fact remains that there is zero evidence that gender identity is innate, making the central tenets of gender ideology crumble.
But, we already knew this, didn’t we? After all, as the WHO says, gender is just a societal construct.
Sources:
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About Simon LeVay: https://en.wikipedia.org/wiki/Simon_LeVay
Originally published at https://pitt.substack.com/p/is-gender-innate-spoiler-no reproduced by kind permission.
